PROCUSTE1 MUTANTS IDENTIFY 2 DISTINCT GENETIC PATHWAYS CONTROLLING HYPOCOTYL CELL ELONGATION, RESPECTIVELY IN DARK AND LIGHT-GROWN ARABIDOPSIS SEEDLINGS

Plant morphogenesis is dependent on a tight control of cell division a nd expansion. Cell elongation during postembryonic hypocotyl growth is under the control of a light-regulated developmental switch. Light is generally believed to exert its effects on hypocotyl elongation throu gh a phytochrome- and blue-light receptor- mediated inhibitory action on a so far unknown cell elongation mechanism. We describe here a new class of allelic mutants in Arabidopsis, at the locus PROCUSTE1 (prc1- 1 to -4), which have a hypocotyl elongation defect specifically associ ated with the dark-grown developmental program. Normal hypocotyl elong ation is restored in plants grown in white, blue or red light. In agre ement with this, the constitutive photomorphogenic mutation cop1-6, wh ich induces a deetiolated phenotype in the dark, is epistatic to prc1- 2 for the hypocotyl phenotype. Epistasis analyses in red and blue ligh t respectively, indicate that phytochrome B but not the blue light rec eptor HY4, is required for the switch from PRC1-dependent to PRC1-inde pendent elongation. The conditional hypocotyl growth defect is associa ted with a deformation of the hypocotyl surface due to an uncontrolled swelling of epidermal, cortical or endodermal cells, suggesting a def ect in the structure of the expanding cell wall, A similar phenotype w as observed in elongating roots, which was however, independent of the light conditions. The aerial part of mature mutant plants grown in th e light was indistinguishable from the wild type. prc1 mutants provide a means of distinguishing, for the first time, two genetic pathways r egulating hypocotyl cell elongation respectively in dark- and light-gr own seedlings, whereby light not only inhibits hypocotyl growth, but a lso activates a PRC1-independent cell elongation program.